In mammals, glucose and fatty acids are major substrates for cellular energy production. Although fatty acids are dominant substrates for ATP production in adult mouse cardiomyocytes, glucose is also important during the fetal and neonatal periods. Under the aerobic condition, glucose is utilized to generate a small amount of ATP by glycolysis, and pyruvate, a glycolytic metabolite, is converted to acetyl-CoA to enter the TCA cycle resulting in robust ATP production via the mitochondrial oxidative phosphorylation. Recently, we found that β-adrenergic stimulation rapidly promoted the glycolysis without significantly increasing the mitochondrial oxygen consumption in cultured neonatal mouse ventricular cardiomyocytes (NVCMs) in the aerobic condition as assessed with the Extracellular Flux Analyzer as well as the metabolome analyses. Interestingly, the lactate formed from the unutilized pyruvate was secreted into the extracellular solution.　Lactate is known to be involved in the intercellular energy shuttle (Coli cycle) and also signaling via lactate receptors (i.e.: GPR81) on downstream cells. We are currently investigating to uncover the molecular mechanism underlying the catecholamine-induced metabolic modulation and the functional significance of this apparently neonate-specific organ-organ interactions in mouse development.